26 terms

Viral Hepatitis 12-12

OM3 - Blue/Bridges - 2hrs
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Describe Hepatitis A virus in terms of:
1. unique viral properties
2. pathogenic mechanism
3. mechanism of transmission
4. age cohort(s)
5. Global & US prevalence
1. picornavirus. Single serotype (infection->recovery = lifetime immunity). acid stable
2. ingested -> absorbed from SI -> replicates in liver -> secreted into bile -> excreted in stool
3. fecal-oral route (person-person), food (esp shellfish) & water. infected person can shed it for up to 1yr.
4. children > adults
5. high prevalence in africa, south america and asia. low elsewhere. epidemics can occur d/t contaminated food.
Describe Hepatits A in terms of:
1. acute disease presentation
2. potential sequelae
3. diagnostic tests
1. jaundice in adults. in children asymptomatic, milder GI-illness w/o jaundice. rash may occur (fever/rash in children)
2. low mortality, NO chronicity.
Describe the following for Hepatitis A:
1. preventatives & available treatments
1. inactivated vaccine available (HAVRIX, VAQTA). Recc'd for children + travel to endemic areas. NO antivirals available.
Describe Hepatitis B virus in terms of:
1. unique viral properties
2. pathogenic mechanism
3. mechanism of transmission
4. age cohort(s)
5. Global & US prevalence
1. partially dsDNA genome (dane particle).
Hbs-antigen = hep B surface antigen is outer capside. large quantity in blood.
HBc-antigen = inner capsid (not detectable in blood)
HBe antigen = non-structural (detectable in blood)
DNA polymerase = reverse transcriptase (dsDNA -> ssRNA -> dsDNA)
Hbx gene = inhibits p53 & GSK-3b ts, may promote oncogene activation.
2. 30-180 day incubation period (LONG). immune response causes most of the damage.
3.blood, sexual contact
4. adults most common
5. high prevalence in africa, asia
Describe Hepatits B in terms of:
1. acute disease presentation
2. potential sequelae
3. diagnostic tests
1.
2. higher mortality rate. can cause acute fulminant, persistence leading to cirrhosis, hepatocellular carcinoma.
Recovery is prolonged. carrier state/chronicity can develop esp in infected newborns.
3. acute = HBsAg, total anti-HBc, IgM anti-HBc, HBeAg
recovery = total anti-HBc, anti-HBs, anti-HBe
chronic = HBeAg, HBsAg, total anti-HBc
Describe the following for Hepatitis B:
1. preventatives & available treatments
1. subunit vaccine (energix-B, recombivax HB), cloned HBs gene. 3 dose series.

Rx = interferon alpha, nucleotide analogues (lamivudine, adefovir, entecavir, telbivudine)
Describe the serologic results for the following states of HBV infectivity:
1. acute hep B
2. persistent carrier
3. recovery
4. immunization w/o infection
1. HBsAg, HBeAg, anti-HBc IgM, anti-HBc-IgG
2. HBsAg, Anti-HBc IgG, +/- HBeAg, anti-HBe
3. anti-HBc IgG, anti-HBs
4. anti-HBs
Describe Hepatitis D virus in terms of:
1. unique viral properties
2. pathogenic mechanism
3. mechanism of transmission
4. age cohort(s)
5. Global & US prevalence
1. defective satellite virus/viroid.
RNA genome is a ribozyme
2. uses outer coat protein of HBV as capsid.
3. acquired by co-infection or super-infection
5. worldwide prevalence
Describe Hepatits D in terms of:
1. acute disease presentation
2. potential sequelae
3. diagnostic tests
1.Increases severity of HBV infection
2. likelihood of fulminant hepatitis, chronicity
Describe Hepatitis C virus in terms of:
1. unique viral properties
2. pathogenic mechanism
3. mechanism of transmission
4. age cohort(s)
5. Global & US prevalence
1. flavivirus
2. HIGH replication rate (10 billion/day)
widespread liver infection < 50% hepatocytes
high mutation rate w/quasispecies, mutant swarm
3. IV drug abuse, sexual
4. adults more common, higher prevalence in IV drug users & hepophilia pt's
5. high world wide, moderate prevalence in US
Describe Hepatits C in terms of:
1. acute disease presentation
2. potential sequelae
3. diagnostic tests
1.
2. chronic/persistent infection very likely. worse in alcohol abusers.
3. 1st anti-HCV 2nd HCV RNA -> med eval if both (+)
Describe the following for Hepatitis C:
1. preventatives & available treatments
1. NO vaccine
Rx = PEG-interferon + protease inhibitor + ribavirin
Describe Hepatitis E Virus
found primarily in developing countries.
Leading worldwide cause of waterborne hepatitis.
Disease and transmission similar to Hepatitis A.
Vaccine in clinical trials.
Describe Hepatitis G Virus
Flavivirus, related to Hepatitis C virus.
Describe HAV in terms of:
1. source of virus
2. route of transmission
3. chronic infection
4. prevention
5. treatment
6. prognosis
1. feces
2. fecal-oral
3. NO
4. immunization
5. IgG
6. excellent
Describe HBV in terms of:
1. source of virus
2. route of transmission
3. chronic infection
4. prevention
5. treatment
6. prognosis
1. blood/blood-derived/body fluids
2. percutaneous/mucosal/sexual
3. yes, esp infants
4. immunization
5. IF/RTI
6. if chronic, variable outcome
Describe HCV in terms of:
1. source of virus
2. route of transmission
3. chronic infection
4. prevention
5. treatment
6. prognosis
1. blood/blood-derived/body fluids
2. percutaneous/mucosal/sexual
3. yes
4. risk behavior modification, blood donor screening
5. IF/Ribavirin/Protease inhibitor
6. if chronic, variable outcome
Describe HDV in terms of:
1. source of virus
2. route of transmission
3. chronic infection
4. prevention
5. treatment
6. prognosis
1. blood/blood-derived/body fluids
2. percutaneous/mucosal/sexual
3. yes
4. same as B
5. same as B
6. if chronic, variable outcome
Describe HEV in terms of:
1. source of virus
2. route of transmission
3. chronic infection
4. prevention
5. treatment
6. prognosis
1. feces
2. fecal-oral
3. no
4. ensure safe drinking water
5. none
6. good
What are the agents used in treatment of hepatitis B virus?
Entecavir
Tenofovir
Lamivudine

Interferon-alfa
What are the agents used in treatment of hepatitis C virus?
peg interferon-alfa + ribavirin + telaprevir or boceprevir (protease inhibitors)
Explain the following for entecavir/tenofovir/lamivudine:
1. mechanism of action
2. toxicity/adverse effects
1. Inhibit HBV DNA polymerase
- **Compete with natural substrates and terminate viral DNA replication
*Require activation to triphosphate form
2. long term dosing req'd
cost
viral resistance
what marks the endpoint of treatment for HBV?
in HBeAg (+) chronic hepatitis = HBeAg seroconversion (antibody production)

HBeAg (-) = HBsAg loss, not established
what pt population can interferon not be used to treat HBV?
pt's w/decompensated cirrhosis
Explain the following for interferon alfa:
1. mechanism of action
2. toxicity/adverse effects
1. turns on gene expresssion of proteins w/antiviral effects -> decreased viral penetration, synthesis of mRNA, translation, viral assembly

2. Neuropsychiatric (depression, suicidal ideation), flu-like symptoms, anemia, neutropenia, enchances autoimmune dz
Explain the following for Ribavirin:
1. mechanism of action
2. toxicity/adverse effects
1. unknown, may inhibit RNA polymerase

2. dose dependent, reversible anemia - d/t extravascular hemolysis
pregnancy cat. X
- strict contraception